Development of Sarcocystis in mule deer transmitted through dogs and coyotes

1983 ◽  
Vol 61 (12) ◽  
pp. 2904-2912 ◽  
Author(s):  
J. P. Dubey ◽  
T. P. Kistner ◽  
Gayle Callis

Tissues from 13 experimentally inoculated mule deer (Odocoileus hemionus) from Oregon, studied by G. Hudkins and T. P. Kistner in 1976 and L. D. Koller, T. P. Kistner, and G. Hudkins in 1977, were reexamined. The following additional information on Sarcocystis hemionilatrantis was obtained. Two types of meronts were found in deer necropsied between 29 and 41 days postinoculation (DPI). Type 1 meronts were in capillaries in adrenal glands, kidney, lymph node, lung, choroid plexi, and spleen; meronts were 20.5 × 13.5 μm (14−32 × 10−20 μm; n = 26) and contained 20 to 35 nuclei. Type 2 meronts were found in macrophages in muscular tissues; these meronts were 20 × 14 μm (10−35 × 7−19 μm; n = 7) and contained 10 to 60 merozoites. Sarcocysts were seen in three deer at 63, 65, and 90 DPI. At 63 and 65 DPI sarcocysts were immature and their walls were thin (< 1 μm) and smooth. At 90 DPI, sarcocysts were up to 525 μm long and 50 μm wide; the sarcocyst wall was 1 to 2 μm thick and cross striated. In the same deer another type of mature sarcocyst was also seen; sarcocysts were up to 825 μm long, the walls were 2 to 4 μm thick and lacked cross striations. Two additional 3-day-old deer were inoculated orally with sporocysts from the feces of a dog fed meat from a mule deer from Montana naturally infected with Sarcocystis sp. Deer No. 1, fed 107 sporocysts, was killed at 14 DPI and deer No. 2, fed 5 × 106 sporocysts, was killed at 24 DPI. At 14 DPI, meronts were found in capillaries and arteries in the lung, heart, and spleen; the meronts were 26.5 × 20 μm (14−39 × 14−25 μm; n = 31) and contained up to 100 nuclei. At 24 DPI, intravascular meronts were found in the spinal cord, hepatic lymph node, kidney, thyroid gland, and mesenteric lymph node. In addition, meronts were found in macrophages in muscular tissues; these meronts were 16 × 10 μm (10−28 × 7−14 μm; n = 10) and contained up to 40 nuclei.

2020 ◽  
Vol 158 (6) ◽  
pp. S-505
Author(s):  
Kazuki Horiuchi ◽  
Masaaki Higashiyama ◽  
Suguru Ito ◽  
Rina Tanemoto ◽  
Shin Nishii ◽  
...  

1999 ◽  
Vol 80 (10) ◽  
pp. 2757-2764 ◽  
Author(s):  
Christina J. Sigurdson ◽  
Elizabeth S. Williams ◽  
Michael W. Miller ◽  
Terry R. Spraker ◽  
Katherine I. O’Rourke ◽  
...  

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer’s patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.


2021 ◽  
Author(s):  
Vittorio Maselli ◽  
et al.

Additional information about the numerical modeling, bathymetric profiles, cross sections along type 1 and type 2 bedforms, a 3-D view of the study area, seafloor bathymetry and thickness map of post-salt deposits, and morphology of sediment waves seaward of the fan.<br>


2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 150-150
Author(s):  
Tadayoshi Hashimoto ◽  
Tomoki Makino ◽  
Makoto Yamasaki ◽  
Koji Tanaka ◽  
Yasuyuki Miyazaki ◽  
...  

Abstract Background Although neoadjuvant chemotherapy (NAC) has recently became a standard treatment for locally-advanced esophageal squamous cell carcinoma (ESCC), residual pattern of cancer cells in resected specimen after NAC has not been clarified yet. Methods A total of 120 patients with cT3 or T4 ESCC who underwent curative esophagectomy after NAC and achieved grade2 as histological efficacy between 2000–2016 were analyzed. We classified the pattern of residual tumor into 4 categories; Type 1: Shallow remnant (between mucosa and submucosa), Type 2: Central remnant (between submucosa and muscularis propria), Type 3: Deep remnant (between muscularis propria and adventitia), and Type 4: diffuse remnant (between mucosa/submucosa and muscularis propria/adventitia) and examined its relationship with clinicopathological factors and prognosis. Results The tumor remnant type was categorized as follows; Type 1/Type 2/Type 3/Type 4: = 49/33/9/29 cases. Forty-five cases had no residual cancer cells in the mucosal layer. The positivity rate of lymphatic invasion was similar between 4 categories, while the positivity of venous invasion was significantly higher in Type 3 and 4 as compared to Type 1 or 2 (P = 0.04). Regarding the pattern of recurrence, lymph node recurrence was more common in Type 1 (69%) and Type 2 (83%) compared to Type 3 (50%) or Type 4 (38%) (P = 0.29). Notably, more patients with Type 3 or 4 developed pleural dissemination or distant metastasis as compared with those with Type 1 or 2 [pleural dissemination: Type 1/2/3/4: 0%/0%/50%/38% (P = 0.029), distant metastasis: Type 1/2/3/4: 31%/13%/50%/88%, (P = 0.11)]. No significant difference in 2-year recurrence-free survival rate was identified among 4 categories (Type 1/2/3/4: 65.9%/78.0%/74.1%/71.8%, P = 0.757). Conclusion The most common pattern of residual tumor after NAC for advanced ESCC was shallow remnant although approximately forty percent of cases inversely showed tumor disappearance at least in mucosal layer. Lymph node metastases was the predominant pattern of disease recurrence in patients with the shallow and middle remnant type while deep and diffuse remnant pattern were significantly associated with pleural dissemination and distant metastasis. Disclosure All authors have declared no conflicts of interest.


2021 ◽  
Author(s):  
Vittorio Maselli ◽  
et al.

Additional information about the numerical modeling, bathymetric profiles, cross sections along type 1 and type 2 bedforms, a 3-D view of the study area, seafloor bathymetry and thickness map of post-salt deposits, and morphology of sediment waves seaward of the fan.<br>


1998 ◽  
Vol 80 (07) ◽  
pp. 37-41 ◽  
Author(s):  
Claudine Mazurier ◽  
Christophe de Romeuf

SummaryVon Willebrand disease is characterised by a quantitative (type 1) or qualitative (type 2) decrease in von Willebrand factor (vWF) a multimeric glycoprotein involved in primary haemostasis. The propep-tide of von Willebrand, also named vWF antigen II (vWF:AgII), is released from platelets and endothelial cells and circulates in plasma as a glycoprotein of 100 kD. In the present study, we attempted to determine whether vWF:AgII level may provide information on the synthesis of vWF, specially in patients with von Willebrand disease (vWD). To elucidate that point, we developed an ELISA and quantify the vWF:AgII in normal individuals and in various vWD patients. The propeptide molar concentration was found to be 5nM as compared to 31 nM for mature vWF. In normal individuals, the level of vWF:AgII was significantly decreased in females from O and A blood groups. In type 2 vWD patients the level of plasma vWF:AgII appears normal in the patients with normal level of platelet vWF. In type 2 B vWD characterised by increased affinity of mature vWF for platelet glyco-protein Ib, the vWF:Ag II in contrast to the vWF antigen (vWF:Ag) was not decreased. In type 2A vWD patients the level of vWF:AgII was decreased in patients with absence of high molecular weight vWF in platelets and plasma but normal in patients with increased sensitivity to proteolysis. Finally, in type 1 vWD, some studied patients have a parallel decrease in vWF:AgII and vWF:Ag whereas in others, the vWF:Ag levels were much more affected than corresponding vWF:AgII levels, as observed in some type 2 vWD patients. Thus, in contrast to that already described, the plasma vWF:AgII level cannot discriminate type 1 from type 2 vWD patients. We conclude that the vWF:AgII measurement provides additional information on the mechanisms responsible for vWD and might also contribute to the classification of vWD patients.


Sign in / Sign up

Export Citation Format

Share Document